To elucidate the mechanism of pyrethroid resistance in Helicoverpa armigera, the study explored three possibilities based on deltamethrin as a model pyrethroid; 1) the existence of mutations in the target site of deltamethrin, 2) the existence of variation at the genomic level between insecticide-susceptible and resistant strains, 3) differences in gene expression patterns between the strains. Based on these hypotheses, three levels of resistant strains and a susceptible strain as well as nine Korean field populations were used. As results, 1) any point mutations were not detected in sodium channel gene. 2) based on newly set Korean reference genome (GCA_026262555.1), approximately 3,369,837 and 1,032,689 variants (SNPs and Indels) were revealed from genome and ORFs, respectively. However, any specific variants were not found to be highly correlated with the level of insecticide resistance. 3) based on DEG analysis, some of detoxification enzyme genes were differently expressed particularly cytochrome P450 genes. Therefore, H. armigera possibly acquires deltamethrin resistance through a combination of actions, including over-expression of various detoxification enzymes such as CYP3 subfamilies and cuticular proteins.

The cotton bollworm, Helicoverpa armigera (Hübner) is a serious agricultural pest which has evolved resistance against many chemical classes of insecticides. This species has evolved resistance to the synthetic pyrethroids across its native range and is becoming a truly global pest, after establishing in Brazil and having been recently recorded in North America. A chimeric cytochrome P450 gene, CYP337B3, has been shown to detoxify to fenvalerate and cypermethrin. The CYP337B3 gene has now been detected in different populations around the world, and is even found in South America. This gene is likely to have arisen independently in different geographic locations, probably through selection on pre-existing diversity, and there is ongoing movement of these alleles around the world. The alleles found in Brazil are those most commonly found in Asia, suggesting a potential origin for the incursion into the Americas. This information should be taken into account when devising control strategies for this invasive pest, both in its native range and in the Americas

The common bed bug, Cimex lectularius L. (Hemiptera: Cimicidae), is an ectoparasitic pest that feeds on humans as well as other mammals. We investigate that point mutations on the voltage-sensitive sodium channel are associated with the resistance to pyrethroids. Two point mutations (V419L and L925I) in the voltage-sensitive sodium channel (VSSC) α-subunit gene have been identified in deltamethrin-resistant bed bugs. L925I, located the intracellular loop between IIS4 and IIS5, has been previously found in a highly pyrethroid-resistant populations of whitefly. V419L, located in the IS6 transmembrane segment, is a novel mutation. To establish a population-based genotyping method as a molecular resistance monitoring tool, a quantitative sequencing (QS) protocol was developed. Frequency prediction equations were generated from the plots by linear regression, and the signal ratios were shown to highly correlate with resistance allele frequencies (r2 > 0.993). In addition to QS, the filter contact vial bioassay (FCVB) method was established and used to determine the baseline susceptibility and resistance of bed bugs to pyrethroids. A pyrethroid-resistant strain showed > 9375- and 6990-fold resistance to deltamethrin and λ-cyhalothrin, respectively. Resistance allele frequencies in different bed bug populations predicted by QS correlated well with the FCVB results, confirming the roles of the two mutations in pyrethroid resistance. Taken together, employment of QS in conjunction with FCVB method should greatly facilitate the detection and monitoring of pyrethroid resistant bed bugs in the field.